When the anti-Aβ protofibril antibody Ban2401 was first shown to reduce amyloid deposition in a Phase 2b clinical trial, researchers worried. Was its otherwise exciting cognitive benefit just an artifact of an imbalance of APOE4 carriers between the treatment and placebo groups, caused by regulatory changes during the trial? At the11th Clinical Trials on Alzheimer’s Disease conference, held October 24–27 in Barcelona, investigators allayed some of those concerns. Their subgroup analysis by APOE genotype indicated that the drug effect was likely real. An early look at biomarkers suggests they are adding up toward a treatment effect on Alzheimer’s pathophysiology.
The effect is small and stable, but consistent across several drugs. Researchers at CTAD debated whether it might be manageable by adjusting dosing.
Subgroup analysis addresses APOE4 randomization imbalance, claims treatment with this anti-Aβ protofibril antibody slowed cognitive decline.
With plasma tests performing in AIBL staging, scientists are sharing data across platforms and cohorts, and tackling standardization to avoid time lost to irreproducibility.
Scientists at CTAD were excited about postmortem validation of tau scans and new, more sensitive tracers. Others are exploring practical applications for live imaging of tau pathology.
Large IDEAS data set establishes that PET scans are valuable in clinical practice. Other studies suggest CSF biomarker ratios perform nearly as well.